/pdf/secretory-products-of-macrophages-5cf7rlxshh.pdf

Secretory products of macrophages.

High density lipoprotein metabolism.

Lipoprotein lipase and lipolysis: central roles in lipoprotein metabolism and atherogenesis.

Sensory responses to the taste, smell, and texture of foods help determine food preferences and eating habits. However, sensory responses alone do not predict food consumption. The view that a "sweet tooth" leads to obesity through excess sugar consumption is overly narrow. In reality, there are multiple links between taste perceptions, taste preferences, food preferences, and food choices and the amount of food consumed. Taste responses are influenced by a range of genetic, physiological, and metabolic variables. The impact of taste factors on food intake further depends on sex and age and is modulated by obesity, eating disorders, and other pathologies of eating behavior. Food preferences and food choices of populations are further linked to attitudinal, social, and--probably most important--economic variables such as income. Nutrition education and intervention strategies aimed at improving population diets ought to consider sensory pleasure response to foods, in addition to a wide range of demographic and sociocultural variables.

Taste preferences and food intake

Atherosclerosis is an inflammatory disease. Its lesions are filled with immune cells that can orchestrate and effect inflammatory responses. In fact, the first lesions of atherosclerosis consist of macrophages and T cells. Unstable plaques are particularly rich in activated immune cells, suggesting that they may initiate plaque activation. We have seen a rapid increase in the understanding of the mechanisms that govern the recruitment, differentiation, and activation of immune cells in atherosclerosis. Experimental research has identified several candidate antigens, and there are encouraging data suggesting that immune modulation as well as immunization can reduce the progression of the disease. This review provides an overview of our current understanding of the role of immune mechanisms in atherosclerosis.

Immune mechanisms in atherosclerosis.

https://deepblue.lib.umich.edu/bitstream/handle/2027.42/25560/0000102.pdf?sequence=1

Sweet tooth reconsidered: Taste responsiveness in human obesity

Human monocyte-derived macrophages in culture produced lipoprotein lipase. Although freshly isolated blood monocytes did not secrete much lipase activity, 1 d in culture was sufficient to trigger measureable enzyme production. During 3 wk in culture, maximal activity was attained after 7 d. At all times, the culture medium contained more enzyme activity than did a serum-heparin eluate or a detergent extract of the cell layer. The lipase activity was stimulated by serum and was inhibited by preincubation with antiserum to bovine lipoprotein lipase or when assayed at a high salt concentration. Furthermore, the enzyme bound to a heparin-Sepharose affinity column at physiological ionic strength. Cells cultured from a subject with primary lipoprotein lipase deficiency secreted no detectable enzyme. Since macrophages are prominent components of atherosclerotic lesions in man, their ability to synthesize and secrete lipoprotein lipase may be important to atherogenesis.

/pdf/lipoprotein-lipase-secretion-by-human-monocyte-derived-otke9f8rxm.pdf

Lipoprotein lipase secretion by human monocyte-derived macrophages.

In obese women (n = 16) at their weight, fasting adipose tissue lipoprotein lipase (LPL) activity, obtained by elution with serum and heparin at 4 degrees and 37 degrees C, was inversely correlated to plasma estradiol levels (r = -0.724; P = 0.002) and (r = -0.641; P = 0.010), respectively. Furthermore, fasting postheparin plasma LPL activity during a heparin infusion, showed an even stronger inverse correlation to plasma estradiol when measured at 60 min (r = -0.815; P less than 0.001). None of the above parameters was correlated to the body mass index. Postprandial LPL activity in postheparin plasma, measured 10 min after a heparin injection, showed a strong positive correlation with plasma free testosterone (r = 0.780; P = 0.001). Neither of these parameters was correlated with the body mass index. The origin of this LPL activity is presently unknown but could conceivably represent a pool of LPL from skeletal muscle. Since it has been shown convincingly that estrogen decreases adipose tissue LPL activity in the rat, the present studies strongly suggest that estradiol is a major negative regulator of fasting adipose tissue LPL activity in women.

/pdf/relationship-between-lipoprotein-lipase-activity-and-plasma-4zowbsikty.pdf

Relationship between lipoprotein lipase activity and plasma sex steroid level in obese women.

The enzyme lipoprotein lipase (LPL) is a glycoprotein located on the luminal surface of capillary endothelial cells (see reviews: 1–4). It is bound to a glycosaminoglycan on the endothelium, can be displaced into plasma by intravenous heparin or other polyanions, and binds to heparin-Sepharose gels. The enzyme has an apparent monomeric molecular weight on SDS gel of over 60,000 and 48,300 by sedimentation-equilibrium ultracentrifugation, and probably functions as a dimer in vivo. It has binding sites for heparin, for the cofactor apolipoprotein CII, and for lipid, and has a separate catalytic site for triglyceride hydrolysis. It is inhibited by serine proteases inhibitors, by protamine, and by high ionic strength. The enzyme appears to be synthesized in a number of different parenchymal cells including monocyte-derived macrophages, Kupfer cells, adipocytes, and cells in cardiac and skeletal muscle. The enzyme is secreted from the adipocyte and transported in an unknown fashion to the plasma surface of the capillary endothelial cell, where it has several functions in humans.

Primary Lipoprotein Lipase Deficiency

Obesity is a heterogeneous group of disorders in terms of etiology; time of development; adipose tissue characteristics; metabolic abnormalities; and associated morbidity and mortality from coronary disease. The typical patient at risk for coronary artery disease in middle age develops abdominal obesity with hypertrophic fat cells in young adulthood, has hypertension, hyperglycemia, hypertriglyceridemia, hypercholesterolemia, and decreased high density lipoprotein (HDL)-cholesterol levels. Two common genetic metabolic disorders--noninsulin-dependent diabetes and familial combined hyperlipidemia--both conform to the prototype, accounting perhaps for a substantial amount of the coronary artery disease associated with obesity.

Per-Henrik Iverius

Papers

Sweet tooth reconsidered: Taste responsiveness in human obesity

Lipoprotein lipase secretion by human monocyte-derived macrophages.

Relationship between lipoprotein lipase activity and plasma sex steroid level in obese women.

Primary Lipoprotein Lipase Deficiency

Obesity and common genetic metabolic disorders.